These findings are similar to those observed in another stem cell model of mitochondrial disease (Lorenz et al, 2017) and suggest either that these cells compensated for lower ATP production by reversing the proton flow in the F1Fo ATPase (Abramov et al, 2010) or the presence of other mechanisms such as downregulating oxygen consumption through complex II (Forkink et al, 2014) are active. This evidence concerns the gene DNAH8 and inborn mitochondrial metabolism disorder.